Streptococcus agalactiae and Escherichia coli induce distinct effector γδ T cell responses during neonatal sepsis.

Autor: Witt LT; Department of Immunology, Mayo Clinic, Rochester MN 55901, USA.; Mayo Graduate School of Biomedical Sciences, Mayo Clinic, Rochester, MN 55901, USA., Greenfield KG; Department of Immunology, Mayo Clinic, Rochester MN 55901, USA., Knoop KA; Department of Immunology, Mayo Clinic, Rochester MN 55901, USA.; Department of Pediatrics, Mayo Clinic, Rochester, MN 55901, USA.
Jazyk: angličtina
Zdroj: IScience [iScience] 2024 Apr 05; Vol. 27 (5), pp. 109669. Date of Electronic Publication: 2024 Apr 05 (Print Publication: 2024).
DOI: 10.1016/j.isci.2024.109669
Abstrakt: Neonates born prematurely are vulnerable to life-threatening conditions such as bacterial sepsis. Streptococcus agalactiae (GBS) and Escherichia coli are frequent causative pathogens of neonatal sepsis, however, it remains unclear if these pathogens induce differential immune responses. We find that γδ T cells rapidly respond to single-organism GBS and E. coli bloodstream infections in neonatal mice. Furthermore, GBS and E. coli induce distinct cytokine production from IFN-γ and IL-17 producing γδ T cells, respectively. We also find that IL-17 production during E. coli infection is driven by γδTCR signaling, whereas IFN-γ production during GBS infection occurs independently of γδTCR signaling. The divergent effector responses of γδ T cells during GBS and E. coli infections impart distinctive neuroinflammatory phenotypes on the neonatal brain. Thus, the neonatal adaptive immune system differentially responds to distinct bacterial stimuli, resulting in unique neuroinflammatory phenotypes.
Competing Interests: The authors declare no competing interests.
(© 2024 The Author(s).)
Databáze: MEDLINE